Role of DNA replication in the induction and turn-off of the SOS response in Escherichia coli.
We have studied the role of DNA replication in turn-on and turn-off of the SOS response in Escherichia coli using a recA::lac fusion to measure levels of recA expression. An active replication fork does not seem to be necessary for mitomycin C induced recA expression: a dnaA43 initiation defective mutant, which does not induce the SOS response at non-permissive temperature, remains mitomycin C inducible after the period of residual DNA synthesis. This induction seems to be dnaC dependent since in a dnaC325 mutant recA expression not only is not induced at 42 degrees C but becomes mitomycin C non-inducible after the period of residual synthesis. Unscheduled halts in DNA replication, generally considered the primary inducing event, are not sufficient to induce the SOS response: no increase in recA expression was observed in dnaG(Ts) mutants cultivated at non-permissive temperature. The replication fork is nonetheless involved in induction, as seen by the increased spontaneous level of recA expression in these strains at permissive temperature. Turn-off of SOS functions can be extremely rapid: induction of recA expression by thymine starvation is reversed within 10 min after restoration of normal DNA replication. We conclude that the factors involved in induction--activated RecA (protease) and the activating molecular (effector)--do not persist in the presence of normal DNA replication.
D000903:Antibiotics, Antineoplastic / Q000494:pharmacology; D001426:Bacterial Proteins / Q000235:genetics; D004260:DNA Repair; D004261:DNA Replication; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics*; D005838:Genotype; D016685:Mitomycin; D008937:Mitomycins / Q000494:pharmacology; D009154:Mutation; D011938:Rec A Recombinases; D001616:beta-Galactosidase / Q000235:genetics
D000903:Antibiotics, Antineoplastic; D001426:Bacterial Proteins; D008937:Mitomycins; D016685:Mitomycin; D011938:Rec A Recombinases; D001616:beta-Galactosidase